Clohisy D R, Ramnaraine M L, Scully S, Qi M, Van G, Tan H L, Lacey D L
Department of Orthopaedic Surgery, University of Minnesota Medical School, and University of Minnesota Cancer Center, Minneapolis 55455, USA.
J Orthop Res. 2000 Nov;18(6):967-76. doi: 10.1002/jor.1100180617.
Osteoprotegerin and osteoprotegerin ligand have recently been identified as novel proteins that inhibit and stimulate, respectively, osteoclast formation. We examined the possibility that osteoprotegerin would inhibit cancer-induced osteoclastogenesis and cancer growth in bone. An experimental model was used in which osteolytic tumors are known to stimulate osteoclastogenesis and grow in femora of osteoclast-deficient mice (op/op). Osteoprotegerin treatment decreased the number of osteoclasts by 90% (p < 0.0007) at sites of tumor in a dose-dependent manner and decreased bone tumor area by greater than 90% (p < 0.003). The mechanisms through which osteoprotegerin decreased osteoclast formation in tumor-bearing animals included (a) an osteoprotegerin-mediated, systemic reduction in the number of splenic and bone marrow-residing osteoclast precursor cells, (b) a decrease in the number of osteoclast precursor cells at sites of tumor as detected by cathepsin K and receptor activator of NFkappaB mRNA expression, and (c) a decrease in osteoprotegerin ligand mRNA at sites of tumor. These findings suggest that osteoprotegerin treatment, in addition to having direct antagonistic effects on endogenous osteoprotegerin ligand, decreases the number of osteoclast precursors and reduces production of osteoprotegerin ligand at sites of osteolytic tumor.
骨保护素和骨保护素配体最近被鉴定为分别抑制和刺激破骨细胞形成的新型蛋白质。我们研究了骨保护素抑制癌症诱导的破骨细胞生成和骨内癌症生长的可能性。使用了一种实验模型,其中溶骨性肿瘤已知会刺激破骨细胞生成并在破骨细胞缺陷小鼠(op/op)的股骨中生长。骨保护素治疗以剂量依赖的方式使肿瘤部位的破骨细胞数量减少了90%(p < 0.0007),并使骨肿瘤面积减少了90%以上(p < 0.003)。骨保护素在荷瘤动物中减少破骨细胞形成的机制包括:(a)骨保护素介导的脾脏和骨髓中破骨细胞前体细胞数量的全身性减少;(b)通过组织蛋白酶K和NFκB受体激活剂mRNA表达检测到肿瘤部位破骨细胞前体细胞数量减少;(c)肿瘤部位骨保护素配体mRNA减少。这些发现表明,骨保护素治疗除了对内源性骨保护素配体具有直接拮抗作用外,还能减少破骨细胞前体的数量,并降低溶骨性肿瘤部位骨保护素配体的产生。